It is known that after ischaemia and reperfusion of organs or individual blood vessels with blood, the inflammation mediators that are unavoidably released from damaged tissue or from tissue that is healthy in principle but ischaemically damaged cause platelets and neutrophilic granulocytes (PMN) to be activated. If these two types of blood cell are activated at the same time, platelet-activating factor (PAF) and leukotriene B4 (LTB4) are synthesised and released, which may selectively and synergistically activate the endothelium of the respective organ venules and also the macrovenous luminal endothelium to contract and open its intercellular spaces. As a result, the outflow of plasma components (e.g. clotting factors, complement factors and platelets) into the respective interstitial space of the organs in question is greatly increased. At the same time, PAF and LTB4 promote the stickiness of the platelets and PMN at the respective endothelium. As sticky leukocytes can damage the endothelium by releasing aggressive compounds (e.g. proteolytic enzymes, oxygen radicals, hypochlorous acid, etc.) and activated platelets on the surface become catalysts of a fibrin formation extending around them by binding and arranging the clotting cascade, inflammatory reactions occur on the wall and in the lumen of affected blood vessels, leading to the formation of clots. These inflammatory processes may spread within organs to smaller blood vessels located downstream. A consequence of inflammations of this kind spreading to the microcirculation is that there is a massive accumulation of white corpuscles inside and around the smallest veins (postcapillary venules) which may induce extensive inflammatory oedema in organs. In addition, there is a high probability that arterioles located in the vicinity will constrict, through the opening of the venular barrier and numerous inflammation mediators, and as a result local bloodflow will be severely restricted. There is also the risk of intravascular thromboses.
If for example organs in a human being suffer from a deficient blood supply during an operation or after explantation, as a rule the inflammatory processes described hereinbefore will generally occur within the respective microvascular systems. In bypass operations in which organ arteries occluded thrombotically or by thickening of the vascular wall are bridged by healthy vascular segments sutured in (often taken from non-essential peripheral veins, less frequently from arteries), there is often the additional problem that the endothelium of the transplanted vascular segments is itself damaged. The high acute restenosing rates of grafts after coronary bypass operations, which have been particularly well studied in this respect (30-40% restenosis even within the first post-operative year!) speak for themselves, and many others become occluded in the decade that follows.
The aim is therefore to protect transplants from the occurrence of the inflammations described above.